Abstract
Chrysoporthe austroafricana is a fungal pathogen that causes the development of stem cankers on susceptible Eucalyptus grandis trees. Clones of E. grandis that are partially resistant and highly susceptible have been identified based on the extent of lesion formation on the stem upon inoculation with C. austroafricana. These interactions have been used as a model pathosystem to enhance our understanding of interactions between pathogenic fungi and woody hosts, which may be different to herbaceous hosts. In previous research, transcriptomics of host responses in these two clones to C. austroafricana suggested roles for salicylic acid and gibberellic acid phytohormone signaling in defense. However, it is unclear how the pathogen infiltrates host tissue and which pathogenicity factors facilitate its spread in the two host genotypes. The aim of this study was to investigate these two aspects of the E. grandis–C. austroafricana interaction and to test the hypothesis that the pathogen possesses mechanisms to modulate the tree phytohormone-mediated defenses. Light microscopy showed that the pathogen occurred in most cell types and structures within infected E. grandis stem tissue. Notably, the fungus appeared to spread through the stem by penetrating cell wall pits. In order to understand the molecular interaction between these organisms and predict putative pathogenicity mechanisms of C. austroafricana, fungal gene expression was studied in vitro and in planta. Fungal genes associated with cell wall degradation, carbohydrate metabolism and phytohormone manipulation were expressed in planta by C. austroafricana. These genes could be involved in fungal spread by facilitating cell wall pit degradation and manipulating phytohormone mediated defense in each host environment, respectively. Specifically, the in planta expression of an ent-kaurene oxidase and salicylate hydroxylase in C. austroafricana suggests putative mechanisms by which the pathogen can modulate the phytohormone-mediated defenses of the host. These mechanisms have been reported in herbaceous plant–pathogen interactions, supporting the notion that these aspects of the interaction are similar in a woody species. This study highlights ent-kaurene oxidase and salicylate hydroxylase as candidates for further functional characterization.
Highlights
The value of model plant–pathogen systems for studying the complexities of plant defense is undeniable
The results suggest that C. austroafricana encounters two different host environments, and we hypothesize that the fungus employs different mechanisms to respond to the phytohormone signaling and other defenses in each host
The macroscopic changes in the stems of E. grandis clones during infection with C. austroafricana were documented over a period of 6 weeks
Summary
The value of model plant–pathogen systems for studying the complexities of plant defense is undeniable. Most of the current knowledge regarding plant defense originates from research conducted in established model systems with herbaceous plants such as Nicotiana spp. and Arabidopsis thaliana (Tsuda and Somssich, 2015), and model systems with woody perennials are scarce. To expand this niche, the interaction of Eucalyptus grandis and Chrysoporthe austroafricana has been established as a model system. The fungal pathogen C. austroafricana causes the development of stem cankers on susceptible E. grandis trees (Roux et al, 2003) It was first discovered in the late 1980s (Wingfield et al, 1989). Damage to plantations caused by this pathogen has largely been limited through the use of E. grandis x E. urophylla hybrids that exhibit increased disease resistance
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